H [Formula: see text] S improves doxorubicin-induced myocardial fibrosis by inhibiting oxidative stress and apoptosis via Keap1-Nrf2

OBJECTIVE: We waimed to investigate whether H [Formula: see text] S can relieve the myocardial fibrosis caused by doxorubicin through Keap1-Nrf2. METHODS: Sprague-Dawley (SD) rats were randomly divided into four groups: normal control group (Control); DOX model group (DOX); H [Formula: see text] S intervention model group (DOX+H [Formula: see text] S); H [Formula: see text] S control group (H [Formula: see text] S). DOX and DOX+H [Formula: see text] S group were injected with doxorubicin (3.0 mg/kg/time) intraperitoneally. Both of the Control group and H [Formula: see text] S groups were given normal saline in equal volume, 2 weeks later, DOX+H [Formula: see text] S and H [Formula: see text] S group were controlled with NaHS (56 [Formula: see text] mol/kg/d) through the abdominal cavity, while the Control and DOX group were injected with normal saline of the same dosage intraperitoneally. RESULTS: Myocardial injury and myocardial cell apoptosis were significantly increased, the H [Formula: see text] S content in myocardial tissue was remarkably down-regulated, the expression levels of MDA, Keap1, caspase-3, caspase-9, TNF- [Formula: see text] , IL1 [Formula: see text] , MMPs and TIMP-1 in rat myocardial tissue was significantly up-regulated ([Formula: see text] 0.05), and the expression levels of GSH, NQO1, Bcl-2 were down-regulated compared with those of control group. The above results can be reversed by the DOX+H [Formula: see text] S group. There is no statistically significant difference between the Control group and the H [Formula: see text] S control group. CONCLUSIONS: These results suggest that H [Formula: see text] S can improve DOX-induced myocardial fibrosis in rats, and the keap1/Nrf2 signaling pathway, oxidative stress, inflammation, and apoptosis may be involved in the mechanism.